We and other investigators have previously shown that iron deficiency, the most common nutritional disorder in children and women of childbearing age, impairs cell-mediated immunity and reduces lymphocyte proliferation by mechanisms that remain elusive. Given the importance of iron for normal functioning of certain enzymes, we postulate that decreased lymphocyte proliferation is due to interrelated but specific defects in some early events in the lymphocyte activation pathways. Some of these events may be related to changes in plasma membrane composition leading to alteration of signal transduction, and others may be iron- dependent and may directly affect DNA synthesis. Our goal is to identify some of these events in a mouse model in which it is possible to induce iron deficiency (by feeding a low iron diet) without concomitant deficiencies in other nutrients that frequently occur in humans. Data to be collected will allow us to understand which events are affected by different degrees of iron deficiency and which ones are not.